AT 1001

AT 1001 (3-300 nM) potently, non-competitively inhibits epibatidine-induced calcium flux in α3β4-transfected HEK cells with an IC₅₀ of 35.2 nM, with no inherent agonist activity^[1].
AT 1001 (10 nM; 500 ms) potently and reversibly inhibits epibatidine-induced inward currents in α3β4-transfected HEK cells, reducing current amplitude by 66% at 10 nM^[1].
AT 1001 (10 μM; 10 min) partially inhibits nicotine-induced [³H]dopamine release from rat NAc synaptosomes, producing 40% inhibition at 10 μM^[1].
AT 1001 exhibits high selectivity for α3β4 nAChRs over most tested receptors and ion channels, with only weak affinity for a small subset of off-targets, including sigma1 receptors (K_i = 84 nM)^[1].
AT 1001 inhibits gliadin-induced intestinal epithelial cell cytoskeletal and tight junction dysfunction, and blocks gliadin- and ZOT analogue-induced paracellular permeability in in vitro intestinal epithelial cell monolayers and diseased human duodenal epithelia^[2].
AT 1001 (1722 nM; 120 s) acts as a partial agonist at rat α3β4 nAChRs expressed in HEK cells, with an EC₅₀ of 1722 nM and 38.1% of nicotine's maximum stimulatory activity^[3].
AT 1001 (10000 nM; 120 s) shows weak partial agonist activity at rat α4β2 nAChRs expressed in HEK cells, with less than 25% of nicotine's maximum stimulatory activity at 10000 nM and an EC₅₀ exceeding 10000 nM^[3].
AT 1001 (91 nM; 15 min) acts as a functional antagonist at rat α3β4 nAChRs expressed in HEK cells, inhibiting epibatidine-induced calcium mobilization with an IC₅₀ of 91 nM^[3].
AT 1001 (276 nM; 15 min) acts as a functional antagonist at rat α4β2 nAChRs expressed in HEK cells, inhibiting epibatidine-induced membrane potential changes with an IC₅₀ of 276 nM, which is threefold higher than its IC₅₀ at α3β4 nAChRs^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.